scholarly journals Methyl Jasmonate and Sodium Nitroprusside Jointly Alleviate Cadmium Toxicity in Wheat (Triticum aestivum L.) Plants by Modifying Nitrogen Metabolism, Cadmium Detoxification, and AsA–GSH Cycle

2021 ◽  
Vol 12 ◽  
Author(s):  
Cengiz Kaya ◽  
Ferhat Ugurlar ◽  
Muhammad Ashraf ◽  
Ahmed Noureldeen ◽  
Hadeer Darwish ◽  
...  

The principal intent of the investigation was to examine the influence of joint application of methyl jasmonate (MeJA, 10 μM) and a nitric oxide–donor sodium nitroprusside (SNP, 100 μM) to wheat plants grown under cadmium (Cd as CdCl2, 100 μM) stress. Cd stress suppressed plant growth, chlorophylls (Chl), and PSII maximum efficiency (Fv/Fm), but it elevated leaf and root Cd, and contents of leaf proline, phytochelatins, malondialdehyde, and hydrogen peroxide, as well as the activity of lipoxygenase. MeJA and SNP applied jointly or singly improved the concentrations of key antioxidant biomolecules, e.g., reduced glutathione and ascorbic acid and the activities of the key oxidative defense system enzymes such as catalase, superoxide dismutase, dehydroascorbate reductase, glutathione S-transferase, and glutathione reductase. Exogenously applied MeJA and SNP jointly or singly also improved nitrogen metabolism by activating the activities of glutamine synthetase, glutamate synthase, and nitrate and nitrite reductases. Compared with individual application of MeJA or SNP, the combined application of both showed better effect in terms of improving plant growth and key metabolic processes and reducing tissue Cd content, suggesting a putative interactive role of both compounds in alleviating Cd toxicity in wheat plants.Main findingsThe main findings are that exogenous application of methyl jasmonate and nitric oxide–donor sodium nitroprusside alleviated the cadmium (Cd)–induced adverse effects on growth of wheat plants grown under Cd by modulating key physiological processes and up-regulating enzymatic antioxidants and the ascorbic acid–glutathione cycle–related enzymes.

Circulation ◽  
1997 ◽  
Vol 95 (9) ◽  
pp. 2303-2311 ◽  
Author(s):  
Nobuhiko Ito ◽  
Josef Bartunek ◽  
Kenneth W. Spitzer ◽  
Beverly H. Lorell

Nitric Oxide ◽  
2009 ◽  
Vol 21 (2) ◽  
pp. 126-131 ◽  
Author(s):  
Darren C. Henstridge ◽  
Brian G. Drew ◽  
Melissa F. Formosa ◽  
Alaina K. Natoli ◽  
David Cameron-Smith ◽  
...  

2006 ◽  
Vol 78 (3) ◽  
pp. 171-177 ◽  
Author(s):  
L. F. A. Huitema ◽  
A. B. Vaandrager ◽  
P. R. van Weeren ◽  
A. Barneveld ◽  
J. B. Helms ◽  
...  

2000 ◽  
Vol 279 (4) ◽  
pp. F728-F735 ◽  
Author(s):  
Mingyu Liang ◽  
Anthony J. Croatt ◽  
Karl A. Nath

We examined whether nitric oxide-generating agents influence expression of heme oxygenase-1 (HO-1) in renal proximal tubular epithelial cells, LLC-PK1 cells, and the mechanisms underlying any such effects. In sublytic amounts, the nitric oxide donor sodium nitroprusside induced HO-1 mRNA and protein and HO activity in a dose-dependent and time-dependent fashion; this induction was specific for nitric oxide since the nitric oxide scavenger carboxy-2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide significantly reduced such induction. The induction of HO activity by sodium nitroprusside, or by another nitric oxide donor, spermine NONOate, was markedly reduced by the iron chelator deferoxamine. Two different thiol-containing agents, N-acetylcysteine and dithiothreitol, blunted such induction of HO by nitric oxide. Downstream products of nitric oxide, such as peroxynitrite or cGMP, were not involved in inducing HO. In higher concentrations (millimolar amounts), sodium nitroprusside induced appreciable cytotoxicity as assessed by lactate dehydrogenase (LDH) release and lipid peroxidation, and both of these effects were markedly reduced by deferoxamine. Inhibition of HO did not affect the cytotoxic effects (measured by LDH release) of sodium nitroprusside. We thus provide the novel description of the induction of HO-1 in renal proximal tubular epithelial cells exposed to nitric oxide donors and provide the first demonstration in kidney-derived cells for the involvement of a redox-based mechanism in such expression. We also demonstrate that, in LLC-PK1 cells exposed to nitric oxide donors, chelatable iron is involved in eliciting the HO-1 response observed at lower concentrations of these donors, and in mediating the cytotoxic effects of these donors when present in higher concentrations.


2021 ◽  
Vol 8 (4) ◽  
pp. 735
Author(s):  
Ana Ecidia de Araújo Brito ◽  
Jessica Suellen Silva Teixeira ◽  
Diana Jhulia Palheta de Sousa ◽  
Evelyn Fátima Lima de Souza ◽  
Gabriel Ito dos Santos Teixeira ◽  
...  

The aim of this work was to evaluate the attenuating effect of the nitric oxide donor (sodium nitroprusside-NPS) on the ecophysiological responses of corn plants (Zea mays L.) submitted to copper toxicity. The corn seeds of the K9606 VIP3 variety were soaked for 48 hours in Germitest with solution containing treatment with sodium nitroprusside Na2 [Fe (CN) 5 NO] 2H2O (0, 200 and 300µM), sodium ferrocyanide Na4Fe (CN) 6 ( 300, 100 and 0 µM) respectively and deionized water (control), sown in buckets with 15 kg of soil incubated for 50 days containing copper concentrations CuSO4.5H2O (0, 60 and 200 mg kg-1). The design consisted of randomized blocks with 12 treatments and 4 repetitions, making a total of 48 plants. in ecophysiological variables: height, leaf area and number of leaves, stem diameter increased by 32, 66% and 11.29% in the treatments with 60 mg kg-1 of copper and 200 mg kg-1 of copper, respectively. There was no effect of treatments on the chlorophyll content measured by the SPAD index and gas exchange. The chlorophyll a fluorescence variables indicate that the concentration of 200 mg kg-1 of copper caused damage to the structure of the PS II reaction center complexes and indicate a slightly protective effect of nitric oxide-NO present in sodium nitroprusside and cyanide present in sodium ferrocyanide, reflecting a smooth functioning of the maximum activity of photosystem II and the electron transport chain.


Clinics ◽  
2008 ◽  
Vol 63 (1) ◽  
pp. 91-96 ◽  
Author(s):  
Ali Emre ◽  
Orhan Bayram ◽  
Bulent Salman ◽  
Sevim Ercan ◽  
Ziya Anadol ◽  
...  

1998 ◽  
Vol 24 (12) ◽  
pp. 1257-1263 ◽  
Author(s):  
Y. Gundersen ◽  
C. O. Corso ◽  
R. Leiderer ◽  
M. Dörger ◽  
P. Lilleaasen ◽  
...  

1994 ◽  
Vol 266 (5) ◽  
pp. H1699-H1705 ◽  
Author(s):  
R. Grocott-Mason ◽  
S. Fort ◽  
M. J. Lewis ◽  
A. M. Shah

In isolated myocytes and papillary muscles, both nitric oxide, acting through guanosine 3',5'-cyclic monophosphate (cGMP), and cGMP analogues exert a novel effect on myocardial contraction, influencing mainly the onset of relaxation. We studied the effect of the exogenous nitric oxide donor, sodium nitroprusside (0.1-10 microM), in isolated ejecting guinea pig hearts at constant filling pressure, afterload, and heart rate to identify its direct myocardial effects in the whole heart. Sodium nitroprusside induced concentration-dependent increases in coronary flow as well as premature and faster early left ventricular (LV) pressure decline, but did not change end-diastolic or peak LV pressure or peak rate of rise of LV pressure. There was no correlation between changes in coronary flow and LV pressure decline. Sodium nitroprusside effects were inhibited by hemoglobin, which inactivates nitric oxide. The cGMP-independent vasodilator nicardipine also increased coronary flow but did not influence early LV pressure fall. Thus exogenous nitric oxide exerts novel direct myocardial relaxant effects in the isolated ejecting heart, independent of its known vasodilator activity, and without compromising systolic function.


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